Analysis of Caspase-9 and Apaf-1 functions on Chlamydial infection

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K15135
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Bacteriology (including mycology)
• Research Institution: Kindai University
• Principal Investigator: AZUMA Yoshinao 近畿大学, 生物理工学部, 准教授 (90333509)
• Research Collaborator: MD Abdul Aziz ; HAYASAKI Kimie ; NIIGAWA Yuichi ; SHIOMURA Sana ; USHIROKITA Rie
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 肺炎クラミジア / Caspase-9 / アポトーシス / Apaf-1 / NODファミリー / 酵母２－ハイブリッド / 動脈硬化

Outline of Final Research Achievements

Chlamydia is an obligate intracellular bacterial pathogen that replicates solely within a membrane-bound vacuole termed an inclusion. Chlamydia seems to perturb multiple cellular processes of the host, such as, rearrangement of the membrane trafficking system for its intracellular multiplication, and inhibition of host cell apoptosis for persistent infection. In an attempt to clarify host factor involvement in apoptosis regulation, we found that inhibition of Caspase-9 restricted, while Apaf-1 promoted, Chlamydia pneumoniae infection. These opposite contributions were confirmed using caspase-9-/- and apaf-1-/- MEFs. Interestingly, caspase-9 in apaf-1-/- MEFs was activated by chlamydial infection but during the infection caspase-3 was not activated. Moreover the activated caspase-9 was observed within chlamydial inclusions. The sequestration of caspase-9 by chlamydia seems to result in apoptosis repression.

Free Research Field

微生物ゲノム解析